4.3 Other disorders of hemostasis Flashcards
Pt with AML:
what hemostasis disorder to be concerned about?
APL (acute promyelocytic leukemia) –form of AML– can induce DIC with Auer rods
Disorders of fibrinolysis
- mech
- clinical presentation
- list 2 causes
- plasmin overactivity. this results in excessive cleavage of serum fibrinogen, so increased bleeding (just like DIC)
1. radical prostatectomy–release of urokinase activates plasmin
2. liver cirrhosis–decrease in alpha 2-antiplasmin activity (inhibits plasmin)
How can obstetric complications cause DIC?
- tissue factor (tissue thromboplastin) is in amniotic fluid and can leak into mother’s blood.
- TF activates coagulation
Pt with liver cirrhosis:
-how does this affect fibrinolysis
- loss of alpha2 antiplasmin activity decreases inhibitiion of plasmin.
- increased bleeding
Pt with signs that are consistent with DIC.
- what other possible disorder should come to mind?
- what labs to check?
- Plasmin overactivity
- Check D-Dimer and platelet count.
- D Dimer will be increased in DIC but not in plasmin overactivity.
- platelets decreased in DIC (being used up) but normal in plasmin overactivity (b/c plasmin is preventing platelet aggregation)
DIC
- mech
- clinical findings
- lab findings (platelets, PT/PTT, fibrinogen, blood smear, D-Dimer)
- Tx
- disseminated intravascular coagulation
- pathologic activation of coag cascade, caused by a variety of other diseases
- “Yin Yang” since both clots and bleeding occur!
- widespread microthrombi lead to ischemia, infarcts
- use of coag factors/platelets leads to bleeding, esp in mucosa
lab:
- platelets: low
- PT: elevated
- PTT: elevated
- fibrinogen: low (consumed to make clots)
- blood smear: MAHA–schistocytes
- D-Dimer: elevated (“remove band-aid”–D-Dimer is product of splitting cross-linked fibrin in removing clot)
Tx:
- blood transfusion with coag factors
- Treat underlying disease
aminocaproic acid
-blocks activation of plasminogen -Tx in plasmin overactivity disorders
Heparin induced thrombocytopenia
-Tx, and what to be careful of?
- use another anticoagulant/antiplatelet
- But don’t use warfarin! b/c these patients also have increased risk for warfarin skin necrosis.
what is the best screening test for DIC dx?
D Dimer.
Pt with adenocarcinoma
-what hemostasis problem to be concerned with? why?
DIC
-mucin activates coagulation, and adenocarcinomas procude more mucin
alpha-2 antiplasmin -related disorder
-inactivates plasmin -part of normal fibrinolysis–important to limit fibrinolytic effect of plasmin -made in liver -Liver cirrhosis: lack of alpha-2 antiplasmin leads to plasmin overactivity
Plasmin overactivity:
- lab values:
1. PT/PTT
2. bleeding time
3. platelet count
4. D dimer
5. fibrinogen split products
- PT/PTT increased–plasmin destroys coag factors
- increased bleeding time
- normal platelet count (platelets remain in blood b/c plasmin blocks platelet aggregation)
- D Dimer normal (No clots with cross-linked fibrin for plasmin to cleave)
- increased (plasmin cleaves fibrinogen)
Plasmin overactivity disorders -clinical finding -examples -labs (platelets, bleeding time, PT/PTT, D-Dimer) -how to differentiate from DIC?
Excess plasmin: 1. excessive cleavage of serum fibrinogen, decreasing platelet aggregation 2. Plasmin destroys coag factors -leads to bleeding, similar to DIC -ex: 1. radical postatectomy–releases urokinase, activating plasmin 2. Liver cirrhosis–reduced production of alpha-2 antiplasmin labs: -platelets: normal -bleeding time: increased (less platelet aggregation) -PT/PTT: elevated. (plasmin destroys coag factors) -D-Dimer: none (fibrin was never formed. as opposed to high D-Dimer in DIC) Tx: aminocaproic acid–blocks activation of plasminogen
Plasmin overactivity:
-tx?
Aminocaproic acid
-blocks activation of plasminogen
Pt who gets his prostate removed.
-what about hemostasis to be concerned about
- Possible overactivity of plasmin (overactive fibrinolysis) from release of urokinase (which acts like tPa)
- increased bleeding
